Wound Care Flashcards
What does skin consist of?
cells, fibers, and an extracellular matrix
how thick is the outer epidermis?
.06-.6mm
Five layers of the outer epidermis
stratum corneum stratum lucidum stratum granulosum stratum spinosum stratum basale
Functions of the outer epidermis
physical/chemical barrier regulates fluid light touch sensation thermoregulation excretion vitamin D production appearance
Stratum corneum
20-30 cells thick
3/4 thickness of the dermis
made of dead keratinocytes
Stratum Lucidum
few layers of flattened dead keratinocytes
they appear clear in microscope
ONLY in palms and soles of feet
What do Langerhans cells do?
bind antigens
Stratum granulosum
3-5 rows flattened cells
increasing concentrations of keratin & Langerhans cells
Stratum spinosum
several rows mature keratinocytes
keratinocytes look spiny
contains Langerhans cells
Stratum Basale
single row of keratinocytes that continuously divide and produce keratin.
Keratin is attached to dermis via basement membrane containing melanocytes and Merkel cells
What is keratin?
a protective protein
How thick is the inner dermis?
2-4 mm thick
How many layers in inner dermis & what are they?
2 layers that are highly vascular:
Papillary dermis & Reticular dermis
Papillary dermis
loosely woven fibers embedded in gelatinous matrix
Blisters occur at the junction of papillary dermis and basement membrane
Reticular dermis
dense, irregularly arranged connective tissue
Name a certain type of cell the dermis contains
fibroblasts that produce collagen, elastin, macrophages, and WBCs
Functions of the dermis
supports/nourishes epidermis houses epidermal appendages (hair, nails, glands) infection control thermoregulation sensation
What does the subcutaneous tissue consist of?
adipose tissue
fascia
Another name for subcutaneous tissue
hypodermis
Adipose tissue
highly vascular, loose CT
stores fat to provide energy, cushion, insulation
Fascia
fibrous CT
separates & surrounds structures
facilitates movement between adjacent structures
3 types of wounds
superficial
partial-thickness
full-thickness (subcutaneous & subdermal
Superficial wounds
only affect the epidermis
Partial thickness wounds
involve epidermis and part of the underlying dermis
Full thickness wounds
through epidermis and dermis to the subcutaneous layer
Further classifications of full thickness wound
subcutaneous-into subcutaneous tissue
sub dermal- tendons, mm, or bone are involved
3 phases of wound healing
Inflammation
Proliferation
Maturation
Inflammation phase of wound healing & how long it lasts
allows body to control blood loss, fend off bacterial invasion, and signal cells needed to repair
1-10 days
Vascular response (Inflammation stage)
Increased permeability of vessel walls causes local edema.
Platelets aggregate to control blood loss
Chemotactic agents attract cells needed for wound repair.
Cellular Response (Inflammation stage)
WBCs go to site to destroy bacteria/debris
Proliferation phase of wound healing & how long it lasts
builds new tissues & restores epithelial integrity
3-21 days but can start within 48 hours of injury
Angiogenesis (proliferation phase)
buds from blood vessel walls grow into affected area, eventually connecting to form new blood vessels
Granulation tissue (proliferation phase)
temp. latticework of CT that fills defect from removal of debris during inflammatory phase.
fibroblasts proliferate & migrate across wound bed.
As angiogenesis forms new vessels, stimulus for fibroblast proliferation DECREASES
Wound contraction (proliferation phase)
fibroblasts–> myofibroblasts that contain actin
Pull wound margins together
Greater in full thickness wounds
Linear wounds contract faster than square or rectanglular.
Circle wounds contract SLOWEST
Epithelialization (proliferation phase)
as defect is filled w/granulation tissue, epithelial cells begin to multiply and go across wound bed.
Epithelialization is slowed by low oxygen and thick debris.
Moist clean wound bed facilitate migration
Maturation & how long it lasts
reorganizes scar tissue to reach max strength & function.
7 days- 2 years
Maturation phase: rosy scar vs. pale scar
rosy pink: remodeling
pale scar: full remodeled
A mature scar has how much of the original tissue’s strength?
80%
Types of wound closure
Primary intention
Secondary intention
Tertiary intention
Primary intention
simplest & fastest
incision is clean
edges are physically approximated (decreases distance keratinocytes must migrate)
heal best if there is low tension across wound & good vasculature
What is Secondary Intention
When wound edges can’t be approximated
severely contaminated wounds may also be allowed to close by secondary intention
What is needed for secondary intention?
granulation tissue must be built to fill wound defect
wound contraction
more time & energy needed
creates more scar tissue
Tertiary intention (aka delayed primary closure)
combo of primary/secondary intention
can be used to decrease chance of infection
wound is initially cleansed then observed for a few days
Once wound is clean, it is surgically closed
What can cause abnormal wound healing?
absence of inflammation chronic inflammation hypogranulation hypergranulation hypertrophic scarring keloids contractures dehiscence
Causes for absence of inflammation
high dose steroids
malnourished
elderly
immune system dysfunction
Can use E stim of phys. agents to promote inflammation
Causes for chronic inflammation
Presence of foreign body repetitive mechanical trauma cytotoxic agents (H202, iodine)
What is hypogranulation/
failure to build enough granulation tissue
Hypogranulation is frequent in patients with:
diabetes
malnutrition
Interventions for hypogranulation
prevent epithelial cells from migrating down sides by wiping wound edges w/gauze.
Lightly packing wound defect.
Extreme case: surgical intervention
Hypergranulation
granulation tissue formation continues after wound defect has been filled.
Wound appears overgrowth.
Deters epithelialization because cells have trouble climbing up.
How to prevent hypergranulation
Protect fragile epithelial cells from trauma such as: Inappropriate whirlpool use, maceration, too frequent dressing changes, adhesives, be cautious using hydrocolloid dressings.
How to resolve hypergranulation
pressure over hypergranular tissue causes local ischemia
Silver nitrate
Surgical Excision
Hypertrophic scarring is caused by
overproduction of immature collagen during proliferative & maturation/remodeling phases
Often associated with contractures
Hypertrophic scarring
red, raised, fibrous lesion that stays within confines of the original wound
Usually regress, at least partially w/o intervention
Interventions for hypertrophic scarring
compression garments 23/7 silicone gel sheets over scarred area to break up collagen. Scar mobiliation Steroid injections Surgery
Hypertrophic scarring is more common in wound that:
cross lines of tension in skin
with prolonged inflammatory phase
burns
Keloids
Caused by excessive immature collagen syntheis extend beyond edges of original wound
Rarely regress independently
have growth phase, then stabilization, then intermittent periods of growth later on.
Keloids are often associated with
tissue trauma
familial disposition
Treatment for keloids
steroid injections
surgical excision
Contractures
More common in wounds that cross a join (usually burns)
shortening of scar tissue
Dehiscence
Due to insufficient collagen production or tensile strength.
wound pulls apart
Usually dehisces THEN gets infected
Dehiscence is common in those with
decreased healing ability
longtime steroid user
diabetes mellitus
malnutrition
Treatment for dehiscence
decrease or eliminate infection
protect from stress or tension
